caa a22 4500 445885084 CHVBK 20180317145556.0 cr unu---uuuuu 170323e20110901xx s 000 0 eng 10.1007/s00011-011-0350-5 doi (NATIONALLICENCE)springer-10.1007/s00011-011-0350-5 Potential involvement of CCL23 in atherosclerotic lesion formation/progression by the enhancement of chemotaxis, adhesion molecule expression, and MMP-2 release from monocytes [Elektronische Daten] [Chu-Sook Kim, Ji-Hye Kang, Hong-Rae Cho, Thomas Blankenship, Kent Erickson, Teruo Kawada, Rina Yu] Objective: CCL23 [Ckβ8-1/myeloid progenitor inhibitory factor 1 (MPIF1)/macrophage inflammatory protein-3 (MIP3)], a member of the CC chemokine family, is involved in leukocyte trafficking, and implicated in inflammatory diseases. In the present study, we investigated the role of CCL23 in the development of human atherosclerosis, which is characterized by an inflammatory disease. Methods: CCL23 transcripts were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and CCL23 protein by immunohistochemistry and enzyme-linked immunosorbent assay (ELISA). Expression of adhesion molecules was determined by flow cytometry, and matrix metalloproteinase-2 (MMP-2) levels by zymography. Results: Proatherogenic factors such as oxidized low-density lipoprotein (oxLDL) and oxidative stress markedly enhanced CCL23 release from human THP-1 macrophages. CCL23 stimulated chemotaxis of human THP-1 monocytes in a dose-dependent manner and enhanced the expression of adhesion molecule CD11c, as well as release of MMP-2 from the THP-1 monocytes. Moreover, CCL23 expression at the mRNA level was significantly higher in human atherosclerotic lesions than in normal arteries, and CCL23 protein was co-expressed with CD68, a specific marker for macrophages. Circulating levels of plasma CCL23 were higher in atherosclerotic patients than in normal subjects. Conclusion: These findings suggest that CCL23 plays a role in the development of human atherosclerosis. CCL23 may be a useful target for the development of antiatherogenic agents. Springer Basel AG, 2011 Chemokines nationallicence Atherosclerosis nationallicence Macrophages nationallicence Oxidative stress nationallicence Kim Chu-Sook Department of Food Science and Nutrition, University of Ulsan, 680-749, Ulsan, South Korea aut Kang Ji-Hye Department of Food Science and Nutrition, University of Ulsan, 680-749, Ulsan, South Korea aut Cho Hong-Rae Ulsan University Hospital, College of Medicine, University of Ulsan, 680-749, Ulsan, South Korea aut Blankenship Thomas College of Medicine, University of California, 95616, Davis, CA, USA aut Erickson Kent College of Medicine, University of California, 95616, Davis, CA, USA aut Kawada Teruo Graduate School of Agriculture, Kyoto University, 611-0011, Kyoto, Uji, Japan aut Yu Rina Department of Food Science and Nutrition, University of Ulsan, 680-749, Ulsan, South Korea aut Inflammation Research SP Birkhäuser Verlag Basel 60/9(2011-09-01), 889-895 1023-3830 60:9<889 2011 60 11 https://doi.org/10.1007/s00011-011-0350-5 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00011-011-0350-5 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Kim Chu-Sook Department of Food Science and Nutrition, University of Ulsan, 680-749, Ulsan, South Korea aut NATIONALLICENCE 700 1- Kang Ji-Hye Department of Food Science and Nutrition, University of Ulsan, 680-749, Ulsan, South Korea aut NATIONALLICENCE 700 1- Cho Hong-Rae Ulsan University Hospital, College of Medicine, University of Ulsan, 680-749, Ulsan, South Korea aut NATIONALLICENCE 700 1- Blankenship Thomas College of Medicine, University of California, 95616, Davis, CA, USA aut NATIONALLICENCE 700 1- Erickson Kent College of Medicine, University of California, 95616, Davis, CA, USA aut NATIONALLICENCE 700 1- Kawada Teruo Graduate School of Agriculture, Kyoto University, 611-0011, Kyoto, Uji, Japan aut NATIONALLICENCE 700 1- Yu Rina Department of Food Science and Nutrition, University of Ulsan, 680-749, Ulsan, South Korea aut NATIONALLICENCE 773 0- Inflammation Research SP Birkhäuser Verlag Basel 60/9(2011-09-01), 889-895 1023-3830 60:9<889 2011 60 11 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer